In hypovolemic shock, reduced intravascular blood volume causes circulatory dysfunction and inadequate tissue perfusion. Without sufficient blood or fluid replacement, hypovolemic shock syndrome may lead to irreversible cerebral and renal damage, cardiac arrest and, ultimately, death. (See What happens in hypovolemic shock, page 438.) Hypovolemic shock requires early recognition of signs and symptoms and prompt, aggressive treatment to improve the prognosis.
Hypovolemic shock usually results from acute blood loss—about one-fifth of the total volume. Such massive blood loss may result from GI bleeding, internal hemorrhage (hemothorax and hemoperitoneum), or external hemorrhage (accidental or surgical trauma) or from any condition that reduces circulating intravascular plasma volume or other body fluids such as in severe burns. Other underlying causes of hypovolemic shock include intestinal obstruction, peritonitis, acute pancreatitis, ascites and dehydration from excessive perspiration, severe diarrhea or protracted vomiting, diabetes insipidus, diuresis, and inadequate fluid intake.
Signs and symptoms
Hypovolemic shock produces a syndrome of hypotension with narrowing pulse pressure; decreased sensorium; tachycardia; rapid, shallow respirations; reduced urine output; and cold, pale, clammy skin. Metabolic acidosis with an accumulation of lactic acid develops as a result of tissue anoxia as cellular metabolism shifts from aerobic to anaerobic pathways. Disseminated intravascular coagulation (DIC) is a possible complication of hypovolemic shock.
No single symptom or diagnostic test establishes the diagnosis or severity of shock. Characteristic laboratory findings include:
elevated potassium, serum lactate, and blood urea nitrogen levels
increased urine specific gravity (greater than 1.020) and urine osmolality
decreased blood pH and partial pressure of arterial oxygen and increased partial pressure of arterial carbon dioxide.